The increase of adipocytes at the abdominal level is directly related with a condition of insulin resistance and hyperinsulinism. The hyperinsulinemia promotes the release of free fatty acids by the adipocyte and its later hepatic transformation to oxidized LDL, which have a great atherogenic potential. Also, the abdominal adipocytes in response to the increase of free fatty acids, oxidized LDL or any other non-well defined metabolic factor increase the production and release of proinflammatory cytokines such as the tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6), which have shown to be able to reduce the expression and activity of the nitric oxide synthase (eNOS) in human cultivated umbilical endothelium cells, suggesting that this could be the mechanism by which the abdominal obesity is related with endothelial dysfunction. In this sense, we have recently demonstrated that in cultured endothelial cells, the angiotensin II, through receptor AT1, stimulates the TNF-α production, which at the same time activates the metalloproteinase 2, enzyme which induces changes in the endothelium structure and in the stability of the atherosclerotic plaque. This effect of angiotensin II is mediated by the AT1 receptor, since we have shown that the CANDESARTAN inhibited the production of TNF-α induced by Angiotensin II.